The fact that the adult brain is very plastic is often held up as evidence against the idea that many psychological, cognitive or behavioural traits are innately determined. At first glance, there does indeed appear to be a paradox. On the one hand, behavioural genetic studies show that many human psychological traits are strongly heritable and thus likely determined, at least in part, by innate biological differences. On the other, it is very clear that even the adult brain is highly plastic and changes itself in response to experience.

The evidence on both sides is very strong. In general, for traits like intelligence and personality characteristics such as extraversion, neuroticism or conscientiousness, among many others, the findings from genetic studies are remarkably consistent. Just as for physical traits, people who are more closely related resemble each other for psychological traits more than people with a more distant relationship. Twin study designs get around the obvious objection that such similarities might be due to having been raised together. Identical twins tend to be far more like each other for these traits than fraternal twins, though the family environment is shared in both cases. Even more telling, identical twins who are raised apart tend to be pretty much as similar to each other as pairs who are raised together. Clearly, we come fairly strongly pre-wired and the family environment has little effect on these kinds of traits.

Yet we know the brain can “change itself”. You could say that is one of its main jobs in fact – altering itself in response to experience to better adapt to the conditions in which it finds itself. For example, as children learn a language, their auditory system specialises to recognise the typical sounds of that language. Their brains become highly expert at distinguishing those sounds and, in the process, lose the ability to distinguish sounds they hear less often. (This is why many Japanese people cannot distinguish between the sounds of the letters “l” and “r”, for example, and why many Westerners have difficulty hearing the crucial tonal variations in languages like Cantonese). Learning motor skills similarly improves performance and induces structural changes in the relevant brain circuits. In fact, most circuits in the brain develop in an experience-dependent fashion, summed up by two adages: “cells that fire together, wire together” and “use it or lose it”.

Given the clear evidence for brain plasticity, the implication would seem to be that even if our brains come pre-wired with some particular tendencies, that experience, especially early experience, should be able to override them.

I would argue that the effect of experience-dependent development is typically exactly the opposite – that while the right kind of experience can, in principle, act to overcome innate tendencies, in practice, the effect is reversed. The reason is that our innate tendencies shape the experiences we have, leading us to select ones that tend instead to reinforce or even amplify these tendencies. Our environment does not just shape us – we shape it.

A child who is naturally shy – due to innate differences in the brain circuits mediating social behaviour, general anxiety, risk-aversion and other parameters – will tend to have less varied and less intense social experience. As a result, they will not develop the social skills that might make social interaction more enjoyable for them. A vicious circle emerges – perhaps intense practice in social situations would alter the preconfigured settings of a shy child’s social brain circuits but they tend not to get that experience, precisely because of those settings. In contrast, their extroverted classmates may, by constantly seeking out social interactions, continue to develop this innate faculty.

This circle may be most vicious in children with autism, most of whom have a reduced level of innate interest in other people. They tend, for example, not to find faces as intrinsically fascinating as other infants. This may contribute to a delay in language acquisition, as they miss out on interpersonal cues that strongly facilitate learning to speak.

A similar situation may hold for children who have difficulties in reading or with mathematics. Dyslexia seems to be caused by an innate difficulty in associating the sounds and shapes of letters. This can be traced to genetic effects during early development of the brain, which may cause interruptions in long-range connections between brain areas. This innate disadvantage is cruelly amplified by the typical experience of many dyslexics. Learning to read is hard enough and requires years of practice and active instruction. For children who have basic difficulties in recognising letters and words, reading remains effortful for far longer and they will therefore tend to read less, missing out on the intensive practice that would help their brain circuitry specialise for reading.

Though less widely known, dyscalculia (a selective difficulty in mathematics) is equally common and shares many characteristics with dyslexia. The initial problem is in innate number sense – the ability to estimate and compare small numbers of objects. This faculty is present in very young infants and even shared with many other animal species, notably crows. Formal mathematical instruction is required to build on this innate number sense but also crucially relies on it. As with reading, mathematics requires hard work to learn and if numbers are inherently mysterious then this will change the nature of the child’s experience, lessen interest and reduce practice. At the other end of the spectrum, those with strong mathematical talent may gravitate towards the subject, further amplifying the differences between these two groups.

Thus, while a certain type of experience can alter the innate tendency, the innate tendency makes getting that experience far less likely. Brain plasticity tends instead to amplify initial differences.

That sounds rather fatalistic, but the good news is that this vicious circle can be broken if innate difficulties are recognised early enough – by actively changing the nature of early experience. There is good evidence that intense early intervention in children with autism (such as Applied Behaviour Analysis) allows them to compensate for innate deficits and lead to improvements in cognitive, communication and adaptive skills. Similarly intense intervention in children with dyslexia has also proven effective. Thus, even if it is not possible to reverse whatever neurodevelopmental differences lead to these kinds of deficits, it should at least be possible to prevent their being amplified by subsequent experience.

Duff FJ, & Clarke PJ (2011). Practitioner Review: Reading disorders: what are the effective interventions and how should they be implemented and evaluated? Journal of child psychology and psychiatry, and allied disciplines, 52 (1), 3-12 PMID: 21039483

19 Comments

It seems like core psychological traits like intelligence, personality, and psychopathology aren’t very malleable, but secondary ones like skills, attitudes, beliefs, and values are. It’s almost like the distinction between hardware and software.

Yes, it’s not surprising really that the things we recognise as “traits” are by definition, something fairly permanent and unchangeable. (Unlike attitudes, beliefs, skills, etc., as you say). The hardware-software analogy may be valid, to a point anyway. I like to think of traits as the system settings and the skills, beliefs, etc. as the content.

Let’s not forget that differences in brain plasticity themselves are partially under genetic control. As for rGE explanations for variance in traits like IQ, I don’t by them. Why aren’t GE correlations detected by multivariate analysis?

I didn’t know multivariate analyses could check for rGE.. I thought they partitioned the variance between traits into the ACE model.. Could you link to a study were they check for rGE and don’t find it?

IQ is correlated with genes, brain volume, behavior, and the environment. An innatist model would say: genes –> brain volume –> IQ –> behavior –> environment. An rGE model would say: genes –> behavior –> environment … or something along those lines with the environment mediating the relationship between genes and IQ/brain volume. One way to test the rGE model is to decompose the variance for IQ and brain volume and then look at the covariation. See the logic in Betjemann et al. “Genetic Covariation Between Brain Volumes and IQ, Reading Performance, and Processing Speed” or Leewenn et al “A genetic analysis of brain volumes and IQ in children.”

I have an ultra-lame question, but at that point, where do you divide a skill versus a core trait? Some precocious kids talk about how they registered sizable gains on the SAT-M from coursework. You could argue that these experiences are the exception, not the rule, as the study cited below found. However, this research also found that several years of challenging coursework was associated with improvement on the SAT.

Does the SAT-M tap into a largely immutable ‘g’ or is it more of a skills measure from that vantage point?

Personally, I find that spending too much time trying to partition variance precisely is a waste of time, as these figures are not biological constants but highly population-specific. The question is, biologically, what do these values mean? Gene x environment correlations are usually presented as two-hit models – the environmental factor only has an effect on people who are genetically vulnerable, for example. If the genes themselves are influencing the environment that people have, then that should show up as a genetic influence.

You see something like this with hiring of sports coaches and managers. The superstars generally don’t get coaching jobs, and when they do get them, they find them frustrating. Jerry West, for example, was a winning coach with the Lakers, but trying to beat into the heads of average players things that were totally obvious to him was frustrating for him, so he switched to the general manager job where he got to select players.

In baseball, the ideal background for being a manager is believed to have been a marginally talented major leaguer at a difficult position: a journeyman catcher or utility infielder.

“Personally, I find that spending too much time trying to partition variance precisely is a waste of time, as these figures are not biological constants but highly population-specific. The question is, biologically, what do these values mean? Gene x environment correlations are usually presented as two-hit models – the environmental factor only has an effect on people who are genetically vulnerable, for example. If the genes themselves are influencing the environment that people have, then that should show up as a genetic influence”

I imagine that you don’t spend any time trying to partition variance, so what you mean is that it’s a waste of time for others to do so. Why would the population specific nature of heritability estimates make them worthless? Surely such estimates narrow the search for the cause of variance and point which way to look. Anyways, you might be interested in the following paper: Tal (2011) “The Impact of Gene–Environment Interaction and Correlation on the Interpretation of Heritability.” It goes some way in (conceptually) clearing up the nature/nature x nurture debate. (Doesn’t our discussing nature/nature x nurture instead of nature/nurture, say something about the utility of heritability estimates?)

Chuck, I mean (and said) trying to calculate the figures *precisely* is a waste of time. Showing a trait is heritable is indeed very useful and behavioural genetics has shown this convincingly. That has been backed up by the discovery of many individual genetic variants that strongly influence behavioural traits. And showing that a trait can be in some way affected by experience is also useful.

Calculating exactly what the percentages are in various populations doesn’t really help much – they are always going to be very rough estimates anyway. What I was trying to do here was show that experience can be affected by genetics, in individuals, in ways that tend to amplify initial differences. Whether such an effect can be discerned in mathematical estimates of heritability is another matter and it doesn’t bear on whether the effect actually happens – it depends on the design of the study.

So if my kid is born with a pleasant personality and has intrinsic traits of agreeableness, I can beat the shit out of them and still rest at night knowing they will be okay?

Arguments of genetic determinism will never be able to rule out variables. The most resilient of soldiers will come down with a case of shell shock in the trenches. A violent, abusive culture will propagate individuals who fail to achieve self actualization.

It is funny how people read into things. The post I wrote is specifically about how experience can alter the brain. The point I was making was that it tends not to overcome innate preferences because the innate wiring tends to shape the experience, leading people to select ones that reinforce or amplify them. How you go from that, to thinking that beating your agreeable child will not have any consequences is beyond me.

“On the one hand, behavioural genetic studies show that many human psychological traits are strongly heritable and thus likely determined, at least in part, by innate biological differences. On the other, it is very clear that even the adult brain is highly plastic and changes itself in response to experience. ”

Then you hypothesize that:

“The reason is that our innate tendencies shape the experiences we have, leading us to select ones that tend instead to reinforce or even amplify these tendencies. Our environment does not just shape us – we shape it.”

No exceptions, no nod to environmental effects. We just shape our environment.

So abused people simply seek out abuse because they were born with genes that cause them to victimize themselves? Seems the insinuation.

“A child who is naturally shy – due to innate differences in the brain circuits mediating social behaviour, general anxiety, risk-aversion and other parameters – will tend to have less varied and less intense social experience.”

Your hypothesis disregards parenting style?

Autism and dyslexia are very specific. But you seem to imply that all behavior and emotion are simply genetically determined.

Statistically an abused child is FAR more likely to abuse than a non abused child. Genetic brain differences?

You are ascribing opinions to me that I have not stated and do not hold. I try not to insinuate anything – I try to mean precisely what I say. For example, I said “Our environment does not just shape us – we shape it”. Note the word “just” in that sentence – it is included for a reason. I do not as you claim say the environment has no effect on us. Quite the opposite in fact – I tried to make it very clear that brain development involves an intimate interaction with the environment and our patterns of experience. The point of the post is that our innate preferences will tend to shape that experience. Again, I use the phrase “tend to” very deliberately, to (try to) make sure that anyone who reads the post carefully will realise I am NOT excluding environmental effects! And I also specifically do not refer to extreme environmental factors or experiences like neglect or abuse _ I absolutely agree that these can have very large effects. You are arguing against positions that you only imagine I hold.

I apologize, in my fervor i didn’t even notice that ‘just’. That does change the context of the sentence.

i will always take issue with any scientist’s attempt to predict behavioral patterns based on genes in any reliable manner. Environmental stimuli provide much more precise observational patterns than genes ever will in the foreseeable future.

I reason that despite our ability to map the genome, and even make such bold statements as we have found the cancer gene or the gay gene or the violence gene, no single gene will ever prove responsible to 100% of any human behavior or psychology.

You obviously lean more towards genetics, and seem to believe that genetics plays a more important role in human development. Personally I lean more towards environment. Even if the influence was a perfect 50/50 balance between the two, environment will always provide data that makes itself much more easily observable and quantifiable.

I am personally on the autistic spectrum, and I have (adopted) cousins who are as well. My family has never been stable and both my cousins and i grew up in chaotic households. If genes play a significant role in our predisposition for autism, then the environments we lived in catalyzed that predisposition. Autistics hate disorder and chaos in their lives. They like stability. The parents failed to procide that stability. Yet I see plenty of healthy, self actualized individuals who grew up in stable, loving home environments. So to me it seems obvious, my environment created me.

Another example: low value mates, physically unnatrtactive people, can suffer from depression or be very confident. I have observed this. Many European women I meet who are not particularly attractive still have confidence. They grew up in good homes with nice parents who instilled confidence in them. Contrast that with many American women I meet who have unspectacular physical features. They starve themselves, the get tons of plastic surgery.

If Autism is genetic and an autistic simply brings out the autism in themselves by reinforcing their own behaviors in the school yard, who’s to say a depressive does not follow the same pattern? Again we have a scenario where we blame the individual, which always is so much easier than looking at environment.

This is the slippery slope I speak of. If you blame genes for autism, why not A.D.D.? Then all of a sudden shoddy schooling is not a problem so much. Kids are the problem. We don;t feel as compelled to alter our behavior to create a better environment for young children, but instead begin to look for ways to alter the children to accomodate the environment that we create, thus reinforcing power structures that favor adult agendas.

In hunter gatherer societies, none of these problems really existed. Psychopathologies and developmental disorders were not a pressing issue. But the adults did not force the children to adhere to schedules, do monotonous work, live outside of a close nit tribal atmosphere (kids are so very isolated these days.)

Gabriel – first, thank you for sharing your own story. . As you say, I tend to focus on the genetic influences because the scientific evidence for their effects is stronger (e.g., from twin studies, especially for autism). That is a general statement however, about sources of variation in the population – it does not equate to or even really apply to individual cases, where genetic predispositions will interact with experience in shaping the way people are.

Also, no one is “blaming” the genes and certainly not blaming the individuals for carrying some particular genetic variants – I am not saying that “an autistic simply brings out the autism in themselves by reinforcing their own behaviors in the school yard”. That makes it sound like they are choosing to be autistic, which is absurd and not the point I am trying to make at all. The point is to recognise the effects that genetic variants can have on risk for disorders like autism or dyslexia (or ADHD, schizophrenia, etc.) or on general personality traits and also recognise the effects that a person’s innate tendencies can have on their experience. This will hopefully allow intervention to short-circuit this vicious cycle.

Any two twins separated at birth will show as many dissimilarities in personality as similarities. This might vary depending on what criteria you look for, be it autism or anger management or intelligence. But for every bit of evidence you claim supports nature over nurture, I could find contradictory evidence.

Environment provides a much more readily predictable set of data than genes do. When dealing with genetics the variables increase. Which is why I feel when it comes to looking at individuals and helping them, much more productivity could come from observing how their environment effects them.

For instance, I believe that a human will never reach self actualization (total self responsibility, independence, rationality) when they are subjected to hierarchical power structures that impede individuation.

You speak of ‘intervening’ in the cycle, but that also implies that a child must be subjected to interference in their development. This reminds me of the dangers of genetics in general, that we will begin to ‘intervene’ to try and cure people of maladies we find genetic. But the ‘intervention’ simply reinforces power dynamics, the implications that adults know what is best for children and no matter how much they protest there are objective goals we need to achieve through manipulation.

Before we do anything, I believe, it would benefit humankind to stop intervening in individual’s lives, children included. Instead of expecting kids to alter themselves to fit our needs (‘why won’t my child listen to me?!’) why not look in the mirror and ask ourselves if we can admit that we are no less fallible. Maybe then we can provide safe environments for our kids to explore, but not tell them how to explore it.

“Calculating exactly what the percentages are in various populations doesn’t really help much – they are always going to be very rough estimates anyway. What I was trying to do here was show that experience can be affected by genetics, in individuals, in ways that tend to amplify initial differences.”

kjmtchl,

According to Standford Encyclopedia of Philosophy the consensus among philosophers of science (POS) is in agreement with you — an ignominious distinction in my opinion :

“There is something of a consensus in most fields (e.g. philosophy of biology, evolutionary biology, psychology and behavioral genetics) that heritability measures (particularly hb2 measures) only have a very limited use. The consensus among philosophers of biology is that broad heritability measures are uninformative but there are a few dissenting voices (e.g. Sesardic 1993 and 2005) (Heritability)

I guess I am of Sesardic’s mind in this matter.

When it comes to heritability estimates there are two important questions related to the issue of “innateness”: “Does broad heritability imply genetic causation?” and “Does high heritability imply environmental immalleability (give the range of environment prevalent during the time the estimates where made)?” The answer to these is dependent on whether the heritability estimates are “confounded” by gene-envrionement interactions and/or correlations. To the extent they are not, exact percentages are very informative. You can see an illustration of this here: http://www.scribd.com/doc/62132318/15/Lost-in-correlations-Direct-and-indirect-genetic-causes (Table 5.4 p.174, from Sesardic, Making Sense of Heritability.)

Now, you are making the case that the estimates (frequently?) are:

“The evidence on both sides is very strong. In general, for traits like intelligence and personality characteristics such as extraversion, neuroticism or conscientiousness, among many others, the findings from genetic studies are remarkably consistent…. I would argue that the effect of experience-dependent development is typically exactly the opposite….Our environment does not just shape us – we shape it.”

Here, you are referring to (active) GE correlations. Now my points would be:

1) Traits need to be evaluated on a one by one basis to determine the extent to which the genetic variance is independent of environmental variance. In the case of some traits, like IQ, the evidence suggests that the variance is mostly additive and therefore not a function of environmental amplification of the sort you seem to be thinking of.

2) Heritability estimates can be semi-informative as to the nature of possible GE correlations, since for there to be such correlations, genes need to be correlated with the environment. So, for example, if the shared environmental component (C) of an estimate is zero, as it is in the case of many traits, you can rule out, a priori, GE(c) correlations.

3) Even if there are significant GE interactions and correlations, you can still make probabilistic causal accounts of the effects of genes — see my reference to Tal (2011) – which then allows for a quantification of the effects of environmental modifications (again, given the range of environment prevalent during the time that the estimates where made.)

So, as I see it, heritability estimates are at least semi-informative in regards to the question of malleability.